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Mycobacterium tuberculosis: Resistan...

Firmani, Marcia Ann.

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Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates./
作者:	Firmani, Marcia Ann.
面頁冊數:	171 p.
附註:	Chair: Lee W. Riley.
Contained By:	Dissertation Abstracts International63-09B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3063360
ISBN:	0493822208

Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates.
Firmani, Marcia Ann.

Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates. - 171 p.

Chair: Lee W. Riley.

Thesis (Ph.D.)--University of California, Berkeley, 2002.

<italic>Mycobacterium tuberculosis</italic> (<italic>M. tuberculosis </italic>) is the leading infectious cause of death in the adult population worldwide. One factor that makes <italic>M. tuberculosis</italic> such a successful pathogen is its ability to reside within and evade the toxic environment of the host macrophage. Among the major antimicrobial products of macrophages are reactive intermediates of the oxidation of nitrogen (RNI) and the reduction of oxygen (ROI). Since certain strains of <italic>M. tuberculosis</italic> exhibit variation in virulence in humans and animal models, we have sought to determine if a correlation exists between virulence and the ability to resist ROI and RNI.

ISBN: 0493822208Subjects--Topical Terms:

1017734
Biology, Microbiology.

Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates.
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245 1 0 $a Mycobacterium tuberculosis: Resistance to reactive nitrogen and oxygen intermediates.
300 $a 171 p.
500 $a Chair: Lee W. Riley.
500 $a Source: Dissertation Abstracts International, Volume: 63-09, Section: B, page: 4040.
502 $a Thesis (Ph.D.)--University of California, Berkeley, 2002.
520 $a <italic>Mycobacterium tuberculosis</italic> (<italic>M. tuberculosis </italic>) is the leading infectious cause of death in the adult population worldwide. One factor that makes <italic>M. tuberculosis</italic> such a successful pathogen is its ability to reside within and evade the toxic environment of the host macrophage. Among the major antimicrobial products of macrophages are reactive intermediates of the oxidation of nitrogen (RNI) and the reduction of oxygen (ROI). Since certain strains of <italic>M. tuberculosis</italic> exhibit variation in virulence in humans and animal models, we have sought to determine if a correlation exists between virulence and the ability to resist ROI and RNI.
520 $a The majority of TB cases stem from reactivation of latent <italic>M. tuberculosis</italic> infections, which may result from removal of host defense mechanisms that keep <italic>M. tuberculosis</italic> in a persistent state. This suggests that host anti-microbial mechanisms become activated to inhibit replication (bacteriostatic) but do not lead to eradication of the bacteria (bacteriocidal).
520 $a Although certain strains of <italic>M. tuberculosis</italic> are capable of resisting both RNI and ROI, the molecular mechanism(s) involved remain unknown. A previously identified gene (<italic>noxR1</italic>) from <italic> M. tuberculosis</italic> was shown to confer upon recombinant <italic>E. coli </italic> and <italic>M. smegmatis</italic> enhanced resistance to RNI and ROI. Our results revealed that the N-terminus of <italic>noxR1</italic> is essential to confer upon <italic>E. coli</italic> resistance to ASN and H 2O2. Further deletion studies revealed a 30-bp region immediately upstream of the putative <italic>noxR1</italic> start codon that was necessary and sufficient for conferring up to 5 logs greater survival to both <italic> E. coli</italic> and <italic>Salmonella typhimurium</italic> in 1.5 mM H 2O2 and to <italic>E. coli</italic> in 7.5 mM ASN compared to the vector control. Recombinant <italic>E. coli</italic> containing an unrelated 30-bp DNA sequence did not exhibit the enhanced survival phenotype. In addition, a frameshift mutation of the 30 bp sequence maintained the survival phenotype in <italic>E. coli</italic>, suggesting that this 30 bp sequence may be acting at the RNA level. Hence, this 30 bp sequence (designated SasR) may function as a regulatory transcript belonging to a recently described class of regulatory RNA transcripts referred to as small RNA (sRNA). (Abstract shortened by UMI.)
590 $a School code: 0028.
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